Adrenergic responsiveness to insulin hypolycemia results in elevations in circulating epinephrine and norepinephrine. The resulting vascular resistance changes of the normovolemic animal and the influence of angiotension II on splenic norepinephrine release have not been determined. Adult mongrel dogs anesthetized with sodium pentobarbital will have surgical placement of an adreno-femoral shunt, arterial catheter and splenic venous-femoral vein shunt. Adrenal vein, splenic vein and arterial blood samples will be drawn simultaneously and analyzed for epinephrine, norepinephrine and dopamine by a single isotope radiometric enzymatic technique. Splenic venous flow will be monitored electromagnetically and adrenal venous flow measured from adrenal sampling times. Adrenal secretion rates of norepinephrine, epinephrine and dopamine and splenic release or uptake of norepinephrine, epinephrine and dopamine will be determine just prior to and 15, 60, 90 and 120 minutes following crystaline insulin, two units intravenously. Splenic vascular resistance will be calculated at each data point. Three groups of 5-10 dogs each will be studied 1) in resting conditions, 2) with insulin hypoglycemia and 3) insulin hypoglycemia and acute nephrectomy. In a separate set of experiments, venous catheters will be placed in the splenic and left renal veins and a femoral arterial catheter placed in anesthetized dogs. Bilateral innervated carotid sinus preparations will be developed. After baseline samples and data collection, the right adrenal gland will be removed, and the left adrenal denervated. Pulsatile perfusion of the carotid sinuses will be carried out at a frequency of 100, and pulse amplitudes of 10, 20 and 40 mm of mercury. Ten minutes after beginning this pulsatile carotid sinus stimulation, blood samples and data collection will be made. Two groups of crotid sinus animals will be studied, one with a mean carotid sinus pressure of 80 mm Hg, and the other with a mean carotid sinus pressure of 60 mm Hg.